Hi Jörg.

I will put a clip soon in a patient with
hypovolemia and pericardial effusion...it is great how look and what
really is...

With respect to fluid responsive...sadly, like
you know, PPV is not useful in spontaneuosly breathing patients...you
can use passive leg raising test and if patient is in sinus rythm and
change 10 % PPV you can say patient is fluid responsive.
/>Another way, recently published is...more easy, if IVC have
inspiratory collapse the probability of fluid responsive is very
high...

Great work my friend.!

Best

Hello Pablo,

thanks a lot for comment!
You´re
absoloutely right with fluid responsiveness (regarding to your
articles of measurement of stroke volume - by the way: thanks a lot
for your very good articles!!!).
But in this case I couldn´t
measure the LVOT gradient correctly. Ok, there was a little
midventriculare gradient in LV that could be used for measurement, but
because of "swimming" heart there wasn´t a reproducible
LVOT-pw-measurement. No chance to use the suprajugulare view to see
ascending or descending aorta for measurement flow with pw.
So I
used DPP (100 x {PPmax - PPmin / (PPmax + PPmin / 2)}); there was no
variation in pulse pressure curve and no increase of DPP over 13% (I
know, I know, that DPP or Delta down is a method evaluated in
mechanically ventilated patients, but I used it in this case to
eximated fluid response, whether I could improve the clinical
situation of that patient by giving fluid).
The deterioration of
clinical situation was for me the leading arguement not to give more
fluid. Over all: with a correct measurement of LVOT-gradient maybe I
had another result?
In this case I corresponded to the wish of
that patient not to elevated the diagnostic and therapy considering
the infaust progrnosis. So no invasive monitoring any more, no
escalation of therapy.
I don´t know whether there was a lack of
phosphate (peripheral hypoxämia with dyspnoea because of reduction of
2,3-bisphosphoglycerat in erythrocytes with shift to the left of
oxygen-binding curve) or thiamine (type-B- lactic acidosis??) (both
are not rare in patients with underlaying malignant disease) that
could also be a reason for bad clinical situation?? I don´t know./>
Pablo. thank you very, very much for helpful comments!!!/>I posted that vid, because of the fact that I couldn´t put the
pieces together to a whole picture.
Retrospective I think that
there was a distinct hypovolämia with pericardial effusion, and that
the "criterias of tamponade" (collaps of RA, LA and RV;
transtricuspidal flow-variants > 45%) are caused by hypovolaemia
(regarding to your first comment) > so I think that was for me a
pitfall.
Best wishes and best greetings,

Jörg.

Hi Jörg.

A positive fluid challengue means that patient
elevates stroke volume at leasts 15 %, 5 minutes post fluid challenge
(you measure LVOT integral pre and post fluid challenge and this is
all) and this maybe don´t mean a full clinical impact if other
mechanism of shock exists.

Best!

Thanks a lot for comments!!!

The clinical picture was
compatible with pericardial tamponade, but the sonographic picture of
VCI was not! I gave rapidly that patient about 500 ml NaCl 0,9% via
central venous catheter but that increase the clinical afflictions of
that patient (dyspnoea!); but you´re right in echocardiographic
guided monitoring I could see a small decrease of RA- and LA-collaps,
so there was a hypovolaemia. But there was no real positive fluid
responsiveness: tachycardia (ECG) and hypotension was still there
without advance towards betterment.

The patient only wanted
a palliative care management (diffuse hepatic, pulmonary and osseous
metastases and known malignant pleural effusion) without invasive or
non-invasive monitoring.

Best greetings,
Jörg.

An interesting clip, did you approach by draining the fluid, giving IV
fluids, or some other strategy?

Hello Jörg.

About echo I think don´t look like a big
pericardial effusion...measuring in diastole it is a moderate
pericardial effusion (less than 2 cm) and IVC is small and with
inspiratory collapse...so...in this case I think pericardial effusion
exist but is not large and this patient have hypovolemia more
likely.

In have seen that in hypovolemia the pericardial
effusions looks more big and the chambers appear to collapse and this
is not because tamponade but yes because the chambers are poor
filled...

This is the only explanation I have for your
echo...with atypical findings of tamponade. What do you think?/>
Best wishes